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FASEB J. 2017 May;31(5):1792-1795. doi: 10.1096/fj.201601221R. Epub 2017 Jan 18.

Multicellular hypothesis for the pathogenesis of Alzheimer's disease.

Author information

1
Department of Medicine University of California, San Francisco, San Francisco, California, USA; edward.goetzl@ucsf.edu.
2
Jewish Home of San Francisco, San Francisco, California, USA; and.
3
Department of Neurology, Memory and Aging Center, University of California, San Francisco, San Francisco, California, USA.

Abstract

Extensive abnormal interactions among microglia, astrocytes, and neurons of the CNS have been observed in proteinopathic neurodegenerative dementias of the elderly. These multicellular interactions are initiated by insoluble tangles of phosphorylated tau protein and plaques of amyloid peptides. Most research has focused on these neurotoxic proteins, but much less is known about the pathogenic roles of the responding resident and recruited neural cells. Principal interactions among the major 3 sets of CNS cells are herein considered at several levels in relation to cellular phenotypic alterations, mechanisms of cellular communication, and extent of involvement in the pathogenesis of Alzheimer's disease and related proteinopathic dementias. It remains to be determined which of these abnormal neurocellular phenomena are primary events and sufficiently contributory to neurodegeneration to be useful targets for therapy of senile dementias.-Goetzl, E. J., Miller, B. L. Multicellular hypothesis for the pathogenesis of Alzheimer's disease.

KEYWORDS:

astrocytes; microglia; neurodegeneration; neurons; proteinopathic dementia

PMID:
28100644
DOI:
10.1096/fj.201601221R
[Indexed for MEDLINE]

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